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Institute of Experimental and Clinical Pharmacology and Toxicology, Medical Faculty, University of Rostock, Germany
Correspondence: Sabine Böckmann, Institute of Experimental and Clinical Pharmacology and Toxicology, Medical Faculty, University of Rostock, Schillingallee 70, 18055 Rostock, Germany. E-mail: pharma-toxi{at}med.uni-rostock.de
In this article, we analyzed the role of kinins and kinin receptors with respect to the activation of leukocytes. In these cells, the biological effects of kinin peptides are mediated by kinin receptor subtypes B1, B2, or both, depending on species and cell type. In contrast to the other leukocytes, neutrophils contain the complete system for the synthesis and release of bioactive kinins. Consequently, very high concentrations of these peptides can be reached in the close neighborhood of the kinin receptors, in particular at the site of inflammation. Kinins are responsible for many effects in leukocytes including the release of other inflammatory mediators, such as cytokines, prostaglandins, leukotrienes, and reactive oxygen species. Obviously, the potency of kinins to stimulate leukocytes is dependent on the differentiation and especially on the activation stage of these cells. An upregulation of kinin receptors on neutrophils and macrophages appears to be involved in increasing the sensitivity of these cells to kinins at the site of inflammation.
Key Words: kinins inflammatory cells G protein-coupled receptor signal transduction
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